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Approach to heart failure medicos notes-com

Approach to Heart failure - An abnormality of Cardiac structure

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Approach to
Heart Failure
Heart Failure
Heart Failure, is a clinical syndrome in which an
abnormality of cardiac structure or function is
responsible for the inability of the heart to eject
or fill with blood at a rate commensurate with the
requirements of metabolizing tissues
General Etiologies Of Cardiac Failure
1. CORONARY VASCULAR -> ACUTE MI
2. VALVULAR -> AORTIC , MITRAL VALVE DISEASE
3. MYOCARDIAL -> ISCHEMIC CARDIOMYOPATHY
4. HYPERTENSION -> HYPERTENSIVE CRISIS
5. RHYTHM DISTURBANCES -> TACHYCARDIA , INDUCED HF
6. PERICARDIAL -> TAMPONADE , CONSTRICTION
Underlying cardiac disease
Conditions that Conditions that
depress ventricular function restrict filling
CAD RESTRICTIVE C.M.PATHY
HTN PERICARDIAL DISEASE
DCM
Valvular heart disease
Congenital heart disease
Precipitating causes
1. Increased salt intake
2. Non compliance with anti CHF medications
3. Acute myocardial infarction
4. Aggravation of Hypertension
5. Acute arrhythmias
6. Infections and or fever
1. Pulmonary Embolism
2. Anemia
3. Thyrotoxicosis
4. Pregnancy
5. Rheumatic, Viral, and Other Forms of Myocarditis
6. Infective Endocarditis
7. Physical, Environmental, and Emotional Excesses
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Approach to heart failure medicos notes-com

  • 2. Heart Failure Heart Failure, is a clinical syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate commensurate with the requirements of metabolizing tissues
  • 3. General Etiologies Of Cardiac Failure 1. CORONARY VASCULAR -> ACUTE MI 2. VALVULAR -> AORTIC , MITRAL VALVE DISEASE 3. MYOCARDIAL -> ISCHEMIC CARDIOMYOPATHY 4. HYPERTENSION -> HYPERTENSIVE CRISIS 5. RHYTHM DISTURBANCES -> TACHYCARDIA , INDUCED HF 6. PERICARDIAL -> TAMPONADE , CONSTRICTION
  • 4. Underlying cardiac disease Conditions that Conditions that depress ventricular function restrict filling CAD RESTRICTIVE C.M.PATHY HTN PERICARDIAL DISEASE DCM Valvular heart disease Congenital heart disease
  • 5. Precipitating causes 1. Increased salt intake 2. Non compliance with anti CHF medications 3. Acute myocardial infarction 4. Aggravation of Hypertension 5. Acute arrhythmias 6. Infections and or fever
  • 6. 1. Pulmonary Embolism 2. Anemia 3. Thyrotoxicosis 4. Pregnancy 5. Rheumatic, Viral, and Other Forms of Myocarditis 6. Infective Endocarditis 7. Physical, Environmental, and Emotional Excesses
  • 7. Pathogenesis 1. Myocardial cell loss  myocyte hypertrophy and elongation. 2. An increase in ventricular volume (the Starling effect) helps maintain cardiac output (CO), but at the cost of increasing ventricular filling pressures. 3. The increase in diastolic stretch and pressure produces further damage stretch-induced myocyte death (apoptosis)
  • 8. CARDIAC OUTPUT SYMPATHETIC DISCHARGE REMODELLING INC.FORCE RATE PRELOAD AFTERLOAD DEC. RENAL BLD FLOW RAA. ACTIVATION CARDIAC OUTPUT SYMPATHETIC DISCHARGE DEC. RENAL BLD FLOW INC.FORCE RATE PRELOAD AFTERLOAD RAA. ACTIVATION CARDIAC OUTPUT SYMPATHETIC DISCHARGE DEC. RENAL BLD FLOW
  • 9. Forms of Cardiac Failure 1. Systolic and diastolic failure 2. Low output and high output failure 3. Acute and chronic heart failure 4. Backward and forward failure 5. Left and right heart failure
  • 10. Approach to the patient 1. RESPIRATORY AND OTHER SYMPTOMS 2. Due to inadequate perfusion of peripheral tissues 1. Fatigue 2. Dyspnoea 3. Due to elevated intracardiac filling pressures 1. Orthopnoea 2. PND 3. Peripheral edema
  • 11. Symptoms of heart failure 1. Respiratory Distress 2. Breathlessness- cardinal manifestation of left ventricular failure 3. May present with progressively increasing severity as 1. exertional dyspnea 2. orthopnea 3. paroxysmal nocturnal dyspnea 4. dyspnea at rest 5. acute pulmonary edema.
  • 12. Symptoms. • URINARY SYMPTOMS. 1. Nocturia may occur early in the course of heart failure. 2. Oliguria is a sign of late cardiac failure. • CEREBRAL SYMPTOMS. 1. Confusion, impairment of memory, anxiety, headache, insomnia, bad dreams or nightmares, and, rarely, psychosis with disorientation, delirium, and hallucinations.
  • 13. Symptoms of predominant right-sided Heart Failure 1. Breathlessness is not very prominent because pulmonary congestion is usually absent. 2. Congestive hepatomegaly - dull ache or heaviness in epigastrium. 3. Other gastrointestinal symptoms, including anorexia, nausea, bloating, a sense of fullness after meals, and constipation due to congestion of the liver and gastrointestinal tract. 4. In severe, preterminal heart failure, inadequate bowel perfusion can cause abdominal pain, distention, and bloody stools.
  • 14. Physical examination 1. JVP 2. S3 3. Pulmonary congestion (rales, dullness over pleural effusion) 4. Peripheral edema 5. Hepatomegaly 6. Ascites
  • 15. Laboratory Investigations 1. CBC, ESR 2. Urine routine 3. LFT 4. RFT 5. CXR 6. ECHO 7. Measurement of BNP
  • 16. BRAIN NATRIURETIC PEPTIDE (BNP) • Pre pro-BNP is formed in the ventricles with myocyte stretch • Broken down to N-terminal-pro-BNP (NT-pro- BNP) and BNP. • Highly accurate for identifying or excluding HF with high sensitivity and specificity • BNP - valuable in differentiating cardiac from pulmonary causes of dyspnea
  • 17. Framingham Criteria for Diagnosis of Congestive Heart Failure One major +two minor for diagnosis 1. Paroxysmal nocturnal dyspnea 2. Neck vein distention 3. Rales 4. Cardiomegaly 5. Acute pulmonary edema 6. S3 gallop 7. Increased venous pressure (>16 cmH2O) 8. Positive hepatojugular reflux 9. Weight loss ≥4.5 kg over 5 days' treatment Major Criteria
  • 18. 1. Extremity edema 2. Night cough 3. Dyspnea on exertion 4. Hepatomegaly 5. Pleural effusion 6. Vital capacity reduced by one-third from normal 7. Tachycardia (≥120 bpm) Minor Criteria
  • 19. NYHA GRADING • Class 1 : no symptoms • Class 2 : symptoms with ordinary activity • Class 3 : less than ordinary activity • Class 4 : even at rest
  • 20. Staging of systolic HF 1. STAGE A- ASYMPTOMATIC/ MILD HF NYHA CLASS 1 / 2 2. STAGE B- MILD /MODERATE HF ,NYHA CLASS 2 / 3 3. STAGE C- ADVANCED HF , CLASS 3 / 4 4. STAGE D- REFRACTORY HF ,CLASS 3 / 4 5. SUSTAINED DECOMPENSATION, FREQUENT HOSPITALISATION
  • 21. Conditions That MIMIC CHF 1. Pulmonary disease 1. Chronic bronchitis 2. Emphysema 3. Asthma 2. Other causes of peripheral edema 1. Liver disease 2. Varicose veins 3. Cyclic edema 4. Renal dysfunction
  • 22. General measures 1. Prevent HF 2. Daily measurement of weight 3. Immunization with influenza and pneumococcal vaccines 4. Education of the patient and family 5. Avoid Excessive alcohol, temperature extremes, and tiring trips 6. Meals - small in quantity, frequent 7. Reduce sodium intake
  • 23. Activity 1. Releive anxiety. 2. Physical and emotional rest 3. Anticoagulants, leg exercises, and elastic stockings. 4. Absolute bed rest is rarely required 5. Regular isotonic exercise 6. Weight reduction in obese
  • 24. • Administration of oxygen • Sleep apnoea - nocturnal continuous positive airway pressure • Dialysis or ultrafiltration in patients with severe HF and renal dysfunction • Other mechanical methods - theraputic thoracocentesis or paracentesis . • CORRECTION OF PRECIPITATING FACTORS
  • 25. Measures for symptom relief CONTROL OF EXCESSIVE FLUID Diet Diuretics Thiazide diuretics Loop diuretics Metalazone Potassium sparing diuretics
  • 26. Role of diuretics 1. Rapid relief of symptoms 2. Controls fluid retention 3. Appropriate use of diuretics is the key element in the success of other drugs
  • 27. DIURETICS • THIAZIDE DIURETICS -useful alone or in combination with other diuretics • In chronic mild HF • K+ depletion and metabolic alkalosis • Suited only if GFR >50%of normal • METALAZONE • Site of action and potency similar to the thiazides • Effective in the presence of moderate renal failure • Both metolazone and thiazides potentiate intravenous loop diuretics
  • 28. FUROSEMIDE, BUMETANIDE, AND TORSEMIDE • Useful in all forms of HF, particularly in refractory HF and pulmonary edema. • Effective in patients with hypoalbuminemia, hyponatremia, hypochloremia, and with reductions in glomerular filtration rate • The action may be potentiated by I.V. administration and by the addition of other diuretics
  • 29. POTASSIUM-SPARING DIURETICS • Spironolactone acts by competitive inhibition of aldosterone • Amiloride and triamterene act directly on the distal tubule/collecting duct. • Most effective with loop and/or thiazide diuretics. • Lower dose of spironolactone (25 mg/d), prolong life in patients with advanced HF
  • 30. Prevention of deterioration of cardiac function or drugs increasing survival 1. Angiotensin converting enzyme (ACE inhibitors) 2. Angiotensin receptor blockers 3. Aldosterone blockers 4. Beta adrenoceptor blockers
  • 31. Angiotensin-Converting Enzyme (ACE) Inhibitors 1. Prevention and treatment of HF at almost all stages 2. Slows remodeling . 3. Cardiac output rises 4. Pulmonary wedge pressure falls, 5. Afterload is reduced with no or only mild reduction of arterial pressure. 6. Signs and symptoms of HF are relieved
  • 32. 1. Enhance exercise performance 2. Reduce long-term mortality . 3. Major effect of ACE inhibitors is on inhibition of local (tissue) renin-angiotensin systems. 4. ACE inhibitor should be maintained indefinitely.
  • 33. ACE Inhibitor in cardiac failure Name Starting dose Target Enalapril 1.25-2.5 BD 10 BD Captopril 6.25-12.5 TID 25-50 TId Lisinopril 2.5-5 0D 20-35 OD Ramipril 1.25 -2.5 BD 5 BD
  • 34. ARB 1. Equally effective 2. ACE inhibitor intolerance
  • 35. BETA BLOCKERS Drug Start Target Carvedilol 3.125 bd 25bd Bisoprolol 1.25 od 10 od Metoprolol 12.5 -25 od 200bd • As ADD on therapy with diuretics and ACEI • Improves ejection fraction,exercise tolerance lowers rate ,dec.myo O2 demand,,reduces arrythmias reverse LVH,prevents sudden deaths
  • 36. Use of Beta blockers 1. Optimise volume status 2. Start at lowest possible dose 3. Increase dose gradually 4. Monitor vital signs ,wt , clinical profile
  • 37. Enhancement of Cardiac contractility 1. Digitalis,digoxin oubain 2. Sympatho mimetic amines 3. Phosphodiesterase inhibitors
  • 39. DIGOXIN 1. Positive inotropic response 2. Inhibit Na+, K+-ATPase 3. Effective in systolic HF complicated by atrial flutter and fibrillation and a rapid ventricular rate 4. Does not improve survival in patients with systolic HF and sinus rhythm, it reduces symptoms of HF 5. No value in diastolic HF.
  • 40. Sympathomimetic Amines 1. Dopamine and dobutamine ,dopexamine 2. Act on β-adrenergic receptors 3. Improve myocardial contractility 4. In severe, acute HF 5. Constant intravenous infusion 6. Can be given for several days 7. Used in refractory HF as a “bridge” to cardiac transplantation. 8. “Downregulation” of adrenergic receptors
  • 41. Phosphodiesterase Inhibitors 1. Amrinone,milrinone,enoximone,piroximone,fen oximone 2. Inhibit phosphodiesterase III 3. Positive inotropic and vasodilator actions 4. Administered intravenously 5. Reverse the major hemodynamic abnormalities associated with HF
  • 42. Vasodilators 1. Useful in severe, acute HF with significant systemic vasoconstriction despite ACE inhibitor therapy. 2. Rapid onset and brief duration of action 3. Sodium nitroprusside 4. Intravenous nitroglycerin 20micg/min max 400micg/min 5. Nesiritide iv bolus 2micg/kg+0.01micg/kg/min 6. Combination of hydralazine and isosorbide dinitrate - for chronic oral administration
  • 43. Nesiritide, a recombinant analog of BNP 1. The newest therapeutic option for ADHF. 2. Increase natriuresis, diuresis, and cardiac index 3. Reduce pulmonary capillary wedge pressure, pulmonary artery pressure, pulmonary vascular resistance, and systemic blood pressure in a dose- dependent manner. 4. Reversal of the deleterious neurohormonal response associated,with HF 5. Reduces levels of endothelin 1, aldosterone,and norepinephrine.
  • 44. • Nesiritide is more effective than nitroglycerin in producing rapid and significant reduction of LV filling pressures • Does not require ICU admission or invasive monitoring . • Lower incidence of tachycardia and proarrhythmic effects. • Lessen the need for supportive therapies such as diuretics
  • 45. Survival benefit of different drugs • Those which reduce MORTALITY • Those which Increase MORTALITY • Those without any proved influence on MORTALITY
  • 46. Reduce mortality 1. Beta Blockers 2. A.C.E. Inhibitors 3. Angiotensin Receptor Blockers 4. Spironolactone 5. Amiodarone
  • 47. Drugs increasing Mortality 1. Inotropes&Inotropic dilators 2. Antiarrythmics except 1. betablockers&Amiodarone 3. Calcium Channelblockers 4. High dose Digoxin
  • 48. Diuretics Digoxin(low dose) Nitrate Those without any proved influence on MORTALITY
  • 49. Fluid retention + Assess volume status Beta blockers ACE 1 Diuretic titrate to euvolemic No fluid retention LVEF <40 %
  • 50. VENTRICULAR RESYNCHRONIZATION 1. Intraventricular conduction is depressed in about one-fourth of patients with chronic HF 2. “Resynchronization” with a device that has three pacing leads (right atrium, right ventricle, and cardiac vein, which provides left ventricular stimulation) improve performance in patients with HF 3. Increase ejection fraction
  • 51. MANAGEMENT OF ARRHYTHMIAS 1. Premature ventricular contractions and episodes of asymptomatic ventricular tachycardia are common in advanced HF 2. VT/VF is responsible for about one-half of all deaths 3. Correction of electrolyte and acid-base disturbances
  • 52. Amiodarone 1. Amiodarone, a class III antiarrhythmicis the drug of choice for patients with HF and atrial fibrillation. 2. Implantable automatic defibrillator prevent sudden deaths
  • 53. Anticoagulants 1. Increased risk of pulmonary emboli secondary to venous thrombosis and of systemic emboli secondary to intracardiac thrombi 2. Patients with HF and atrial fibrillation, previous venous thrombosis, and pulmonary or systemic emboli are at high risk 3. Heparin followed by warfarin
  • 54. Management of Diastolic HF 1. HTN regression of LVH important ……ARB,ACE 2. Myocardial ischemia…….. Bblockers ,CCB,nitrates 3. Chronic AF……. restore sinus rythmn,rate control 4. Beta blocker…… slow rate ,reduce O2 demand,lower BP,regress LVH 5. CCB has lusiotropic effect (relaxation enhancing effect) 6. ACE inh. Effect uncertain ……ARB use regress LVH 7. Exercise conditioning….. improves diastolic function ,dynamic isotonic exercise ideal 8. Better Prognosis 9. Bad prognosis-Older age ,males ,lower ej.fraction,ass,CAD,DM,impaired renal function
  • 55. Management Of ADHF • Administration of oxygen • Morphine sulfate • Mechanical ventilation is indicated • A sitting position improves pulmonary function. • Placing the patient on strict bed rest and reducing pain and anxiety decrease cardiac workload.
  • 56. 1. Intravenous inotropes and vasodilators - The combination of an intravenously administered vasodilator such as nitroglycerin, niseritide, or of a phosphodiesterase inhibitor together with a sympathomimetic amine 2. Hemodynamic monitoring cvc,swan ganz catheter,O2 saturation 3. Extracorporeal ultrafiltration and hemofiltration- Acute hemodialysis and ultrafiltration may be effective, especially in the patient with significant renal dysfunction and diuretic resistance ,removes i.v fluid
  • 57. 1. Mechanical circulatory supports 2. Devices 1. Counter pulsation device(Intra aortic baloon pump and non invasive counter pulsation) 2. Cardiopulmonary assist devices 3. Left ventricular assist devices
  • 58. • In hospitalized patients with refractory HF, therapy to be guided by hemodynamic measurements by a balloon flotation (Swan-Ganz) catheter • The goal is to achieve pulmonary capillary wedge pressure of 15 to 18 mmHg • Right atrial pressure of 5 to 8 mmHg • Cardiac index >2.2 L/min per m2 • Systemic vascular resistance of 800 to 1200 dyne · s/cm5.
  • 59. SURGICAL THERAPY • CARDIAC TRANSPLANTATION best predictor peak O2 consumption with maximal exercise (VO2max)NI >20ml/kg/min,<10ml/kg/min ……transplantation ideal • Novel surgeries – Ventricular remodelling surgeries – Dynamic cardiomyoplasty – Mitral valve repair
  • 60. NEWER Rx MODALITIES FOR ADHF 1. BALOON COUNTER PULSATION – INTRAAORTIC BALOON PUMP 2. VAD – PULSATILE LOW FLOW VAD 3. PACING – BIVENTRICULAR PACING , AV SEQUENTIAL PACING
  • 61. B N P analogue Nesiritide Endopeptidase inhibitor(ACE+neutral peptidases) Omapatrilat NEWER DRUGS
  • 62. Pimobendan,Levosibendan • LEVOSIBENDAN is a novel agent with inotropic properties developed specifically for the management of ADHF. • It acts by sensitizing troponin C to calcium Calcium Sensitiser
  • 63. Endothelin receptor antagonist BOSENTAN TEZOZENTAN Effective in acute coronary syndromes, acute renal failure and acute HF. • Indirectly improve contractility while decreasing pulmonary capillary wedge pressure.
  • 64. • VASOPRESSIN ANTAGONISTS (V2 RA) Tolvaptan, Lixiraptan ,Coniraptan – CAN BE USED AS ADJUVANT to DIURETIC IN ADVANCED HF • ENOXIMONE –TYPE 3 PDEI – PA Pr. MONITORING REQUIRED – LV FILLING PRESSURE > 15 mm Hg – IDEAL INOTROPE FOR PATIENT ON ß BLOCKERS
  • 65. PROGNOSIS 1. Depends primarily on the nature of the underlying heart disease 2. Presence or absence of a precipitating factor 3. Prognosis can be estimated by observing the response to treatment. 4. When patients can be rendered free of congestion, survival may be 80% at two years.
  • 66. 1. High BUN (>43 mg/dL) is the best single predictor of inhospital mortality 2. Severely depressed ejection fraction<15% 3. Inability to walk on level at normal pace>3min 4. Low SBP (<115 mm Hg) 5. High serum creatinine (SCr) levels (>2.75 mg/dL). 6. Elevations in circulating levels of B-type natriuretic peptide (BNP) 7. Cardiac necrosis marker troponin I
  • 67. When all available therapeutic measures have been exhausted, comfort care, with continued infusions of inotropic agents, diuretics, and the administration of anxiolytics and analgesics should be considered.